左旋精氨酸对吸烟大鼠肺部炎症干预作用机制的研究

目的：探讨左旋精氨酸（L－Arg)干预吸烟大鼠肺部炎症变化的机制。方法：99只Wistar大鼠随机分为对照组，吸烟组，吸烟＋L－Arg组，实验大鼠计数肺泡灌洗液（BALF）中的中性粒细胞数，并测定其中IL－8的含量，观察肺组织的病理变化。结果：（1）BALF中的中性粒细胞数；吸烟组显高于对照组（P＜0．05），吸烟＋L－A rg组高于对照组，低于吸烟组（P＜0．05），BALF中IL－8含量；吸烟组在1周，2周及2个月显高于对照组（P＜0．05），并与中性粒细胞数呈正相关，同时，吸烟＋L－Arg组IL－8的含量较吸烟组显减少（P＜0．05），（2）HE染色显示，吸烟组肺组织有明显的炎症细胞浸润，吸烟1周后，支气管上皮细胞纤毛不完整，至2个月伴有支气管上皮细胞脱落，吸烟＋L－Arg组肺组织炎症变化及上皮细胞损伤较累，结论：吸烟引起的肺炎症症和损伤与IL－8含量升高有关；L－Arg干预可能通过抑制IL－8的产生而减轻吸烟引起的上述变化。

The Mechanism of Effect of L-arginine on Inflammation of Lung in Smoking Rats

Objective: To explore the therapeutic effect of L-arginine on inflammation and damage caused by smoking. Methods: 99 Wistar rats were randomly divided into three groups: control group, smoking group and treatment group (smoking + L-arginine). The number of neutrophils and the concentration of IL-8 in bronchial alueolar lavage fluid (BALF) were determined. HE staining was used to observe the pathological changcs in lung tissues. Results: The number of neutrophils in BALF in the smoking group was significantly higher than that of the control group. It was higher in the treatment group than that in the control group, but lower when compared with the smoking group (P< 0.05 ). The level of IL-8 in the smoking group was slgnificantly increased after smoking for 1 week, 2 week and 2 months(P<0.05 ) and had a positive correlation with the neutrophil count (r=0.732, P<0.05 ). It was significantly lower in the treatment group than that in the smoking group(P<0.05 ). HE staining showed that there was obvious inflammatory cells infiltration in the lung tissues and loss of cilia in airway epithelium in the smoking group. But the Pathological change was much gentler in the treatment group. Conclusion: The inflammation and damage in lung tissue caused by cigarette smoking may be related with the increase of IL- 8 in BALF. L-arginine treatment can inhibit the production of IL-8 and reduce the pathological damage caused hy smoking.